Neuroscience Flashcards
Define encephalitis.
Inflammation of the brain parenchyma.
Explain the aetiology / risk factors of encephalitis.
Causes:
- VIRAL - e.g. HSV, herpes zoster, mumps, adenovirus, coxsackie, echovirus, enteroviruses, measles, EBV, HIV, rabies (Asia), Nipah (Malasia), arboviruses transmitted by mosquitos (Jap B encephalitis - Asia, St Louis and West Nile encephalitis - USA)
- NON-VIRAL - e.g. syphillis, Staphylococcus aureus
- IMMUNOCOMPROMISED - e.g. CMV, toxoplasmosis, Listeria
- AUTOIMMUNE OR PARANEOPLASTIC - associated with antibodies - e.g. anti-NMDA or anti-VGKC
Summarise the epidemiology of encephalitis.
7.4 in 100,000 in UK
Recognise the presenting symptoms of encephalitis.
- Can be mild and self-limiting
- Subacute onset (hours to days)
- Headache
- Fever
- Vomiting
- Neck stiffness
- Photophobia - i.e. symptoms of meningism (meningoencephalitis)
- Behavioural changes
- Drowsiness
- Confusion
- History of seizures
- Focal neurological symptoms - e.g. dysphagia, hemiplegia
- DETAILED TRAVEL HISTORY
Recognise the signs of encephalitis on physical examination.
- Reduced level of consciousness with deteriorating GCS
- Seizures
- Pyrexia
- Neck stiffness
- Photophobia
- Kernig’s test positive
- Hypertension
- Bradycardia
- Papilloedema
- Focal neurological signs - e.g. dysphagia, hemiplegia
- Minimental examination may reveal cognitive or psychiatric disturbances
NB: Raised intracranial signs and meningism signs.
Identify appropriate investigations for encephalitis and interpret the results.
- Bloods
- MRI / CT
- Lumbar Puncture
- EEG
- Brain Biopsy
Bloods
- FBC - high lymphocytes
- U&E - SIADH may occur
- Glucose - compare with CSF glucose
- Viral serology
- ABG
MRI / CT
- Excludes mass lesion
- HSV produces characteristic oedema of the temporal lobe on MRI
Lumbar Puncture
- High lymphocytes
- High monocytes
- High protein
- Glucose usually normal
- CSF culture difficult
- Viral PCR now first line
EEG
- Epileptiform activity
- E.g. spiking activity in temporal lobes
Brain Biopsy
- Rarely performed
Define epilepsy.
> 2 seizures.
Seizure = paroxysmal synchronised cortical electrical discharges.
Focal Seizures
- Localised to specific cortical regions
- Temporal lobe, frontal lobe, occipital, complex partial
- Simple partial - does not affect consciousness
- Simple complex - does affect consciousness
Generalised Seizures
- Affect consciousness
- Tonic clonic, absence attacks, myoclonic, atonic (drop attacks), tonic seizures
Explain the aetiology / risk factors of epilepsy.
Result from an imbalansce in the inhibitory and excitatory currents (Na+ or K+) or neurotransmittors (glutamate or GABA) in the brain. Can be precipitated or are cryptogenic.
Precipitants:
- Flashing lights
- Drugs
- Sleep deprivation
- Metabolic
Idiopathic.
Primary Syndromes
- Idiopathic generalized epilepsy
- Temporal lobe epilepsy
- Juvenile myoclonic epilepsy
Secondary Seizures (Symptomatic)
- Tumour
- Infection - meningitis, encephalitis, abscess
- Inflammation - vasculitis, multiple sclerosis
- Toxic / metabolic - sodium imbalance, hyperglycaemia, hypoglycaemia, hypocalcaemia, hypoxia, porphyria, liver failure
- Drugs - alcohol withdrawal, benzodiazepine withdrawal
- Vascular - haemorrhage, infarction
- Congenital anomalies - cortical dysplasia
- Neurodegenerative disease - Alzheimer’s disease
- Malignant hypertension or eclampsia
- Trauma
Common Seizure Mimics
- Syncope
- Migrane
- Non-epileptiform seizure disorder (e.g. dissociative disorder)
Summarise the epidemiology of epilepsy.
Common.
1% of general population.
Peak age of onset is in early childhood or in elderly.
Recognise the presenting symptoms of epilepsy.
Obtain history from a witness as well as a patient.
Key features from history to determine seizure semiology:
- Rapidity of onset?
- Duration of episode?
- Any alteration of consciousness?
- Any tongue-biting or incontinence?
- Any rhythmic synchronous limb jerking?
- Any post-ictal period?
- Drug history - alcohol, recreational drugs
FOCAL SEIZURES
- Frontal lobe focal motor seizures - motor convulsions, Jacksonian march (spasm spreads from mouth or digit), post-ictal flaccid weakness (Todd’s paralysis)
- Temporal lobe seizures - aura (visceral and psychic symptoms, fear or deja-vu sensation), hallucinations (olfactory, gustatory)
- Frontal lobe complex partial seizures - loss of consciousness, automatisms, rapid recovery
GENERALISED SEIZURES
- Tonic-clonic (grand mal) - vague symptoms before attack (irritability), tonic phase (generalised muscle spasm), clonic phase (repetitive synchronous jerks), faecal or urinary incontinence, tongue biting, impaired consciousness, lethargy, confusion, headache, back pain, stiffness afterwards
- Non-convulsive status epilepticus - acute confusional state, fluctuating, difficult to distinguish from dementia
Recognise the signs of epilepsy on physical examination.
Depends on aetiology, usually normal between seizures.
Look for focal abnormalities indicative of brain lesions.
Identify appropriate investigations for epilepsy and interpret the results.
Bloods
- FBC, U&E, LFTs
- Glucose, Ca2+, Mg2+
- ABG, toxicology screen
- Prolactin - transient increase shortly after a true seizure
EEG
- Helps confirm or refute the diagnosis
- Assists in clarifying the epileptic syndrome
- Usually performed inter-ictally and often normal and does not rule out epilepsy
- Ictal EEGs combined with video telemetry are more useful but requires adequate facilities
CT / MRI
- For structural, space-occupying and vascular lesions
Others
- Particularly for secondary seizures according to suspected aetiology
- E.g. lumbar puncture, HIV serology
Generate a management plan for epilepsy.
STATUS EPILEPTICUS: seizure lasting longer than 30 minutes, failure to regain consciousness
- Early treatment has higher success - give at 5-10 minutes
- Resuscitate and protect airway, breathing and circulation
- Check glucose and give if hypoglycaemic
- Consider thiamine
- IV lorazepam or IV/PR diazepam - repeat once after 15 minutes if needed
- Reoccur or fail to respond- give IV phenytoin (15mg/kg) under ECG monitoring
- Alternative IV agents - phenobarbitone, levetiracetam, sodium valproate
- If these measures fail, consider general anaesthesia - requires intubation and mechanical ventilation
- Treat cause - e.g. correct hypoglycaemia or hyponatraemia
- Check plasma levels of all anticonvulsants
PHARMACOLOGICAL TREATMENT
- Only start anti-convulsant therapy after >2 unprovoked seizures
- Lamotrigine or carbamazepine - 1st line focal seizures
- Sodium valproate - 1st line generalised seizures
- Others - phenytoin, levetiracetam, clobazam, topiramate, gabapentin, vigabatrin, ethosuximide (absence)
- Start treatment with single anti-epileptic drug (AED)
PATIENT EDUCATION
- Patient education
- Avoid triggers - e.g. alcohol
- Encourage seizure diaries
- Recommend supervision for swimming or climbing
- Driving only permitted if seizure free for 6 months
- Women of childbearing age should be counselled regarding possible teratogenic effects of AEDs and should consider taking supplemental folate to limit the risk
- Drug interactions can limit the effectiveness of oral contraception
SURGERY
- For refractory epilepsy
- Removal of definable epileptogenic focus - determined from detailed EEG, intra-cortical recordings, ictal SPECT, neuropsychometry
- Vagus nerve stimulator
Identify the possible complications of epilepsy (including status epilepticus) and its management.
- Fractures with tonic-clonic seizures
- Behavioural problems
- Sudden death in epilepsy (SUDEP)
- Complications of AEDs
SE of phenytoin = gingivial hypertrophy
SE of carbamazepine = neutropenia, osteoporosis
SE of lamotrigine = Stevens-Johnson syndrome
Summarise the prognosis for patients with epilepsy.
50% remission at 1 year
Mortality 2 in 100,000 per year
Directly related to seizure or secondary to injury
Define extradural haemorrhage.
Aka epidural haematoma.
Collection of blood that forms between the inner surface of the skull and outer layer of the dura, which is called the endosteal layer.
Associated with a history of head trauma and associated skull fracture.
Explain the aetiology / risk factors of extradural haemorrhage.
Causes:
- Traumatic skull fracture - to a temple just lateral to the eye - temporal or parietal bone
- Laceration of middle meningeal artery and vein
- Tear in dural venous sinus
Differentials - epilepsy, carotid dissection, carbon monoxide poisoning.
Summarise the epidemiology of extradural haemorrhage.
2% of all head injuries
15% of all fatal head traumas
Recognise the signs of extradural haemorrhage on physical examination.
- Deteriorating consciousness after head injury
- No initial loss of consciousness
- Initial drowsiness post injury seems to have resolved
- Lucid interval pattern - lasts a few hours to a few days before reducing GCS from raised ICP
- Severe headache
- Vomiting
- Confusion
- Seizures
- Hemiparesis with brisk reflexes and upgoing plantar
If bleeding continues:
- Ipsilateral pupil dilation
- Coma deepening
- Bilateral limb weakness
- Breathing becomes deep and irregular due to brainstem compression
- Death following period of coma due to respiratory arrest
- Bradycardia and high BP are late signs
Recognise the presenting symptoms of extradural haemorrhage.
- Deteriorating consciousness after head injury
- No initial loss of consciousness
- Initial drowsiness post injury seems to have resolved
- Lucid interval pattern - lasts a few hours to a few days before reducing GCS from raised ICP
- Severe headache
- Vomiting
- Confusion
- Seizures
- Hemiparesis with brisk reflexes and upgoing plantar
If bleeding continues:
- Ipsilateral pupil dilation
- Coma deepening
- Bilateral limb weakness
- Breathing becomes deep and irregular due to brainstem compression
- Death following period of coma due to respiratory arrest
- Bradycardia and high BP are late signs
Identify appropriate investigations for extradural haemorrhage and interpret the results.
CT
- Shows haematoma lens-shaped / biconvex
- Rounded blood shape
NB: Sickle-shaped subdural haematoma as touch dural attachments to skull keep it more localized
Skull X-RAY
- Normal
- Fracture lines crossing course of middle meningeal vessels
LUMBAR PUNCTURE IS CONTRAINDICATED.
Define meningitis.
Inflammation of the leptomeningeal (pia mater and arachnoid) coverings of the brain, most commonly caused by infection.
Aseptic meningitis - characterised by clinical and laboratory evidence for meningeal inflammation and negative routine bacterial culture
Mollaret’s meningitis - recurrent benign lymphocytic meningitis
Explain the aetiology / risk factors of meningitis.
Bacterial
- Neonates - Group B streptococci, Escherichia coli, Listeria monocytogenes
- Children - Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae
- Adults - Neisseria meningitidis (meningococcus), Streptococcus pneumonia, tuberculosis
- Elderly - Streptococcus pneumoniae, Listeria monocytogenes
Viral
- Enteroviruses
- Mumps
- HSV
- VZV
- HIV
Fungal
- Cryptococcus - associated with HIV infection
Aseptic Meningitis
- Enterovirus, mycobacteria, fungi, spirochetes
- Autoimmune - e.g. Sarcoidosis, Behcet’s disease, Systemic lupus erythematosus
- Malignancy - lymphoma, leukaemia, metastatic carcinomas
- Medication - NSAIDs, trimethoprim, azathioprine
Mollaret’s Meningitis
- 50% exhibit transient neurological manifestations
- HSV-2
- Large granular plasma cells on Papnicolaou’s stain, PCR for HSV DNA
- Treat with acyclovir
Risk Factors:
- Close communities - e.g. dormitories
- Basal skull fractures
- Mastoiditis
- Sinusitis
- Inner ear infections
- Alcoholism
- Immunodeficiency
- Splenectomy
- Sickle cell anaemia
- CSF shunts
- Intracranial surgery
Summarise the epidemiology of meningitis.
Variation according to geography, age, social conditions.
UK Public Health Laboratory Service receives approx 2500 notifications / year.
Recent visitors to Haj (meningococcal serogroup W135).
Epidemics occur in the meningitis belt of Africa (meningococcal serogroup A).